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Increased micronuclei and nuclear abnormalities in buccal mucosa and oxidative damage in saliva from patients with chronic and aggressive periodontal diseases

Background and Objective Periodontal disease is a chronic bacterial infection characterized by connective tissue breakdown and alveolar bone destruction because of inflammatory and immune response caused by periodontopathogens and long‐term release of reactive oxygen species. A high number of reacti...

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Bibliographic Details
Published in:Journal of periodontal research 2015-02, Vol.50 (1), p.28-36
Main Authors: Zamora-Perez, A. L., Ortiz-García, Y. M., Lazalde-Ramos, B. P., Guerrero-Velázquez, C., Gómez-Meda, B. C., Ramírez-Aguilar, M. Á., Zúñiga-González, G. M.
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Language:English
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Summary:Background and Objective Periodontal disease is a chronic bacterial infection characterized by connective tissue breakdown and alveolar bone destruction because of inflammatory and immune response caused by periodontopathogens and long‐term release of reactive oxygen species. A high number of reactive oxygen species result in periodontal tissue damage through multiple mechanisms such as lipid peroxidation, protein denaturation and DNA damage. The aim of this study was to evaluate DNA and oxidative damage in subjects with chronic or aggressive periodontitis and healthy controls. Material and Methods Buccal mucosa cells and whole saliva were collected from 160 subjects, who were divided into three groups: subjects with chronic periodontitis (CP) (n = 58), subjects with aggressive periodontitis (AgP) (n = 42) and a control group (n = 60). DNA damage was determined by counting micronuclei (MN) and nuclear abnormalities (NAs) in exfoliated cells, including binucleated cells, cells with nuclear buds and karyolitic, karyorrhectic, condensed chromatin and pyknotic cells. The degree of oxidative stress was determined by quantifying 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG) in whole saliva. Results Subjects with CP or AgP presented significantly more ( p 
ISSN:0022-3484
1600-0765
DOI:10.1111/jre.12175